Clostridium perfringens-Induced Host-Pathogen Transcriptional Changes in the Small Intestine of Broiler Chickens

Abstract

Clostridium perfringens is an important opportunistic pathogen that may result in toxin-mediated diseases involving food poisoning/tissue gangrene in humans and various enterotoxaemia in animal species. It is a main etiological agent for necrotic enteritis (NE), the most financially devastating bacterial disease in broiler chickens, especially if raised under antibiotic-free conditions. Importantly, NE is responsible for losses of six billion US dollars annually in the global poultry industry. To investigate the molecular mechanisms of C. perfringens-induced pathogenesis in the gut and its microbiome mRNA levels in C. perfringens-infected and non-infected hosts, we used RNA sequencing technology to perform transcriptional analysis of both host intestine and microbiome using our NE model. The growth rate was significantly impaired in chickens infected by C. perfringens. In total, 13,473 annotated chicken genes were differentially expressed between these two groups, with ninety-six genes showing statistical significance (|absolute fold changes| > 2.0, adjusted p value < 0.05). Genes involved in energy production, MHC Class I antigen, translation, ribosomal structures, and amino acid, nucleotide and carbohydrate metabolism from infected gut tissues were significantly down-regulated. The upregulated genes were mainly engaged in innate and adaptive immunity, cellular processes, genetic information processing, and organismal systems. Additionally, the transcriptional levels of four crucial foodborne pathogens were significantly elevated in a synergic relationship with pathogenic C. perfringens infection. This study presents the profiling data that would likely be a relevant reference for NE pathogenesis and may provide new insights into the mechanism of host-pathogen interaction in C. perfringens-induced NE infection in broiler chickens.

Evaluation of Predisposing Factors of Necrotic Enteritis in Experimentally Challenged Broiler Chickens

“…NE triggers an inflammatory response in the intestines of birds [ 32 ] and dysbiosis [ 33 , 34 ], causing energy imbalance and alteration in skeletal muscle growth [ 35 ].…”

“…According to Huang et al [ 47 ] NE lesion scores are higher after one day of CP challenge and the lesions are mild at seven days. After infection with CP, the organism modulates strategies, upregulating protein components, to maintain intestinal integrity and reduce the damage caused by the bacteria [ 35 ].…”

Cannabidiol and Nano-Selenium Increase Microvascularization and Reduce Degenerative Changes in Superficial Breast Muscle in C. perfringens-Infected Chickens

“…As reported, both CBD and nano-Se manifest direct and indirect actions on the same mechanisms of the gut physiological status, particularly the modulation of gut bacterial composition and activities; thus, we speculated that both CBD and nano-Se could be more effective in supporting gut integrity and should thus affect meat properties, especially in challenged birds, as this condition leads to fermentation disturbance, as proven in various models [27][28][29]. For instance, chickens challenged with C. perfringens were shown to have a higher abundance of several foodborne pathogens in the gut, including C. jejuni, E. coli and L. monocylogenes; this treatment also affected the transcript levels of many genes regulating host metabolism [30]. In our previous study [31], in a turkey model, we found that challenging birds with C. perfringens had a significant effect on the sarcoplasmic protein profile of the breast muscle, indicating a strong association between C. perfringens infection and the function of glycolytic enzymes in turkeys, which could lead to significant consequences in cell metabolism [32].…”

Cannabidiol affects breast meat volatile compounds in chickens subjected to different infection models

“…In a study on a meat duck model, it was found that under E. coli -LPS inflammation, there were significant alterations in the cecal microbiota as well as produced SCFAs 15 . In a study on a chicken model, infection with C. perfringens caused an increase in the host gut abundance of several foodborne pathogens, including C. jejuni , E. coli and L. monocylogenes, and affected the transcript levels of a number of genes regulating host metabolism 16 . In another study, a close correlation between cecal C. perfringens and C. jejuni was shown, indicating a potential influence on the final product quality 17 .…”